Fig. 5

The proliferative response of SVZ neuroblasts to a cortical injury is inhibited in the presence of a classical PKC inhibitor that impairs TGF-α release. A Confocal microscopy images of the SVZ of adult mice bearing unilateral cortical injuries and administrated with the classical PKC inhibitor Gö6976 during 7 days. Dotted lines delineate lateral ventricles (LV) borders. Scale bar = 100 μm and 50 μm in the high magnification images. Mechanical cortical lesions were unilaterally performed in the primary cortex of adult male mice. Samples were processed for the immunodetection of the proliferation marker Ki67 and the early neuronal marker doublecortin (DCX). B Graph represents the average ratios obtained when dividing the number of Ki67⁺ cells in ipsilateral SVZ by the number of Ki67⁺ cells in the corresponding contralateral SVZ (considered as 1). Statistical analysis: * p < 0.05. Data are the mean ± S.E.M; n = 6 animals per group, using one-way ANOVA. C. Graph represents the DCX burden as a percentage of SVZ total area. D Graph represents the average ratios obtained when dividing the number of Ki67⁺-DCX⁺ cells in ipsilateral SVZ by the number of Ki67⁺-DCX⁺ cells in the corresponding contralateral SVZ (considered as 1). Statistical analysis: * p < 0.05. Data are the mean ± S.E.M; n = 6 animals per group, using one-way ANOVA. E Levels of TGF-α in the CSF of control and injured mice treated with vehicle or the cPKC inhibitor for 7 days after the injury were obtained after deep anesthesia following the experimental procedure detailed in materials and methods. The levels of TGF-α in non-injured mice (sham) were represented by a dotted line. Statistical analysis: * p < 0.05. Data are the mean ± S.E.M; n = 4–6 animals per group, using a Student´s t-test for equal-variance unpaired samples